Understanding Parinaud’s Syndrome

Parinaud’s syndrome involves dysfunction of the structures of the dorsal midbrain. We investigated the pathophysiology related to the signs and symptoms to better understand the symptoms of Parinaud’s syndrome: diplopia, blurred vision, visual field defects, ptosis, squint, and ataxia, and Parinaud’...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Juan Fernando Ortiz, Ahmed Eissa-Garces, Samir Ruxmohan, Victor Cuenca, Mandeep Kaur, Stephanie P. Fabara, Mahika Khurana, Jashank Parwani, Maria Paez, Fatima Anwar, Hyder Tamton, Wilson Cueva
Formato: article
Lenguaje:EN
Publicado: MDPI AG 2021
Materias:
Acceso en línea:https://doaj.org/article/21fd3b59d5014a1ba5f07bf9a7759a29
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:21fd3b59d5014a1ba5f07bf9a7759a29
record_format dspace
spelling oai:doaj.org-article:21fd3b59d5014a1ba5f07bf9a7759a292021-11-25T16:57:57ZUnderstanding Parinaud’s Syndrome10.3390/brainsci111114692076-3425https://doaj.org/article/21fd3b59d5014a1ba5f07bf9a7759a292021-11-01T00:00:00Zhttps://www.mdpi.com/2076-3425/11/11/1469https://doaj.org/toc/2076-3425Parinaud’s syndrome involves dysfunction of the structures of the dorsal midbrain. We investigated the pathophysiology related to the signs and symptoms to better understand the symptoms of Parinaud’s syndrome: diplopia, blurred vision, visual field defects, ptosis, squint, and ataxia, and Parinaud’s main signs of upward gaze paralysis, upper eyelid retraction, convergence retraction nystagmus (CRN), and pseudo-Argyll Robertson pupils. In upward gaze palsy, three structures are disrupted: the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), interstitial nucleus of Cajal (iNC), and the posterior commissure. In CRN, there is a continuous discharge of the medial rectus muscle because of the lack of inhibition of supranuclear fibers. In Collier’s sign, the posterior commissure and the iNC are mainly involved. In the vicinity of the iNC, there are two essential groups of cells, the M-group cells and central caudal nuclear (CCN) group cells, which are important for vertical gaze, and eyelid control. Overstimulation of the M group of cells and increased firing rate of the CCN group causing eyelid retraction. External compression of the posterior commissure, and pretectal area causes pseudo-Argyll Robertson pupils. Pseudo-Argyll Robertson pupils constrict to accommodation and have a slight response to light (miosis) as opposed to Argyll Robertson pupils were there is no response to a light stimulus. In Parinaud’s syndrome patients conserve a slight response to light because an additional pathway to a pupillary light response that involves attention to a conscious bright/dark stimulus. Diplopia is mainly due to involvement of the trochlear nerve (IVth cranial nerve. Blurry vision is related to accommodation problems, while the visual field defects are a consequence of chronic papilledema that causes optic neuropathy. Ptosis in Parinaud’s syndrome is caused by damage to the oculomotor nerve, mainly the levator palpebrae portion. We did not find a reasonable explanation for squint. Finally, ataxia is caused by compression of the superior cerebellar peduncle.Juan Fernando OrtizAhmed Eissa-GarcesSamir RuxmohanVictor CuencaMandeep KaurStephanie P. FabaraMahika KhuranaJashank ParwaniMaria PaezFatima AnwarHyder TamtonWilson CuevaMDPI AGarticleneurologyparinaudmidbraincollier signpseudo argyll robertson pupilNeurosciences. Biological psychiatry. NeuropsychiatryRC321-571ENBrain Sciences, Vol 11, Iss 1469, p 1469 (2021)
institution DOAJ
collection DOAJ
language EN
topic neurology
parinaud
midbrain
collier sign
pseudo argyll robertson pupil
Neurosciences. Biological psychiatry. Neuropsychiatry
RC321-571
spellingShingle neurology
parinaud
midbrain
collier sign
pseudo argyll robertson pupil
Neurosciences. Biological psychiatry. Neuropsychiatry
RC321-571
Juan Fernando Ortiz
Ahmed Eissa-Garces
Samir Ruxmohan
Victor Cuenca
Mandeep Kaur
Stephanie P. Fabara
Mahika Khurana
Jashank Parwani
Maria Paez
Fatima Anwar
Hyder Tamton
Wilson Cueva
Understanding Parinaud’s Syndrome
description Parinaud’s syndrome involves dysfunction of the structures of the dorsal midbrain. We investigated the pathophysiology related to the signs and symptoms to better understand the symptoms of Parinaud’s syndrome: diplopia, blurred vision, visual field defects, ptosis, squint, and ataxia, and Parinaud’s main signs of upward gaze paralysis, upper eyelid retraction, convergence retraction nystagmus (CRN), and pseudo-Argyll Robertson pupils. In upward gaze palsy, three structures are disrupted: the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), interstitial nucleus of Cajal (iNC), and the posterior commissure. In CRN, there is a continuous discharge of the medial rectus muscle because of the lack of inhibition of supranuclear fibers. In Collier’s sign, the posterior commissure and the iNC are mainly involved. In the vicinity of the iNC, there are two essential groups of cells, the M-group cells and central caudal nuclear (CCN) group cells, which are important for vertical gaze, and eyelid control. Overstimulation of the M group of cells and increased firing rate of the CCN group causing eyelid retraction. External compression of the posterior commissure, and pretectal area causes pseudo-Argyll Robertson pupils. Pseudo-Argyll Robertson pupils constrict to accommodation and have a slight response to light (miosis) as opposed to Argyll Robertson pupils were there is no response to a light stimulus. In Parinaud’s syndrome patients conserve a slight response to light because an additional pathway to a pupillary light response that involves attention to a conscious bright/dark stimulus. Diplopia is mainly due to involvement of the trochlear nerve (IVth cranial nerve. Blurry vision is related to accommodation problems, while the visual field defects are a consequence of chronic papilledema that causes optic neuropathy. Ptosis in Parinaud’s syndrome is caused by damage to the oculomotor nerve, mainly the levator palpebrae portion. We did not find a reasonable explanation for squint. Finally, ataxia is caused by compression of the superior cerebellar peduncle.
format article
author Juan Fernando Ortiz
Ahmed Eissa-Garces
Samir Ruxmohan
Victor Cuenca
Mandeep Kaur
Stephanie P. Fabara
Mahika Khurana
Jashank Parwani
Maria Paez
Fatima Anwar
Hyder Tamton
Wilson Cueva
author_facet Juan Fernando Ortiz
Ahmed Eissa-Garces
Samir Ruxmohan
Victor Cuenca
Mandeep Kaur
Stephanie P. Fabara
Mahika Khurana
Jashank Parwani
Maria Paez
Fatima Anwar
Hyder Tamton
Wilson Cueva
author_sort Juan Fernando Ortiz
title Understanding Parinaud’s Syndrome
title_short Understanding Parinaud’s Syndrome
title_full Understanding Parinaud’s Syndrome
title_fullStr Understanding Parinaud’s Syndrome
title_full_unstemmed Understanding Parinaud’s Syndrome
title_sort understanding parinaud’s syndrome
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/21fd3b59d5014a1ba5f07bf9a7759a29
work_keys_str_mv AT juanfernandoortiz understandingparinaudssyndrome
AT ahmedeissagarces understandingparinaudssyndrome
AT samirruxmohan understandingparinaudssyndrome
AT victorcuenca understandingparinaudssyndrome
AT mandeepkaur understandingparinaudssyndrome
AT stephaniepfabara understandingparinaudssyndrome
AT mahikakhurana understandingparinaudssyndrome
AT jashankparwani understandingparinaudssyndrome
AT mariapaez understandingparinaudssyndrome
AT fatimaanwar understandingparinaudssyndrome
AT hydertamton understandingparinaudssyndrome
AT wilsoncueva understandingparinaudssyndrome
_version_ 1718412824271650816